ArticleJournal of bone and mineral metabolism2015
Interleukin-1-induced acute bone resorption facilitates the secretion of fibroblast growth factor 23 into the circulation.
Article in Journal of bone and mineral metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- FGF-23 as a Biomarker for Carotid Plaque Vulnerability: A Systematic Review.Medical sciences (Basel, Switzerland) · 2025Pooled it
- Interleukin-1 inhibition, chronic kidney disease-mineral and bone disorder, and physical function .Clinical nephrology · 2017Trial
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Effects of dietary myo-inositol supplementation on the expression of fibroblast growth factor 23 (FGF23) and αKlotho in two commercial laying hen strains.Poultry science · 2026Article
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- It is worth the weight: obesity and the transition from monoclonal gammopathy of undetermined significance to multiple myeloma.Blood advances · 2023Review
- Bone marrow sinusoidal endothelial cells are a site of Fgf23 upregulation in a mouse model of iron deficiency anemia.Blood advances · 2023Article
- Review
- Paracrine and endocrine functions of osteocytes.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2023Review
- Desferrioxamine alleviates UHMWPE particle-induced osteoclastic osteolysis by inhibiting caspase-1-dependent pyroptosis in osteocytes.Journal of biological engineering · 2022Article
- The regulation of FGF23 under physiological and pathophysiological conditions.Pflugers Archiv : European journal of physiology · 2022Review
- Roles of osteocytes in phosphate metabolism.Frontiers in endocrinology · 2022Review
- Urinary Potassium Excretion, Fibroblast Growth Factor 23, and Incident Hypertension in the General Population-Based PREVEND Cohort.Nutrients · 2021Article
- Regulation of FGF23: Beyond Bone.Current osteoporosis reports · 2021Review
- Ex vivo Bone Models and Their Potential in Preclinical Evaluation.Current osteoporosis reports · 2021Review
- Article
- Lack of PTEN in osteocytes increases circulating phosphate concentrations by decreasing intact fibroblast growth factor 23 levels.Scientific reports · 2020Article
- Serum hepcidin level, iron metabolism and osteoporosis in patients with rheumatoid arthritis.Scientific reports · 2020Article
- FGF23 at the crossroads of phosphate, iron economy and erythropoiesis.Nature reviews. Nephrology · 2020Review
- p38MAPK controls fibroblast growth factor 23 (FGF23) synthesis in UMR106-osteoblast-like cells and in IDG-SW3 osteocytes.Journal of endocrinological investigation · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 23 (FGF23), a central regulator of phosphate and vitamin D metabolism, is mainly produced by osteocytes in bone and exerts its effects on distant organs. Despite its endocrine function, the mechanism controlling serum FGF23 levels is not fully understood. Here we tested the hypothesis that osteoclastic bone resorption may play a role in regulating circulating levels of FGF23, using a mouse model where injections of interleukin (IL)-1β into the subcutaneous tissue over the calvaria induced rapid bone resorption. A significant amount of FGF23 was detected in the extracts from mouse bones, which supports the idea that FGF23 stays in bone for a while after its production. IL-1β-induced bone resorption was associated with elevated serum FGF23 levels, an effect abolished by pre-treatment with pamidronate. Fgf23 expression was not increased in either the calvariae or tibiae of IL-1β-injected mice, which suggests that IL-1β facilitated the entry of FGF23 protein into circulation by accelerating bone resorption rather than increasing its gene expression. The direct effect of IL-1β on bone was confirmed when it increased FGF23 levels in the conditioned media of mouse calvariae in organ culture. Repeated treatment of the cultured calvariae with IL-1β led to a refractory phase, where FGF23 was not mobilized by IL-1β anymore. Consistent with the in vivo results, treatment with IL-1β failed to increase Fgf23 mRNA in isolated primary osteocytes and osteoblasts. These results suggest that FGF23 produced by osteocytes remains in bone, and that rapid bone resorption facilitates its entry into the bloodstream.
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Registered trials
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